Dopamine attenuates ethanol-induced neuronal apoptosis by stimulating electrical activity in the developing rat retina.

Abstract

Background: Prenatal alcohol exposure causes fetal alcohol spectrum disorders (FASD), primarily through alcohol-induced apoptosis. This study explores the link between ethanol-induced neuronal apoptosis and neural network electrical activity in developing rat retinal ganglion cells, and examines dopamine's protective effects and influence on this activity.

Methods: The study employed a combination of immunohistochemical techniques, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and electrophysiological recordings to assess neuronal apoptosis and neural network activity in the developing rat retinal ganglion cell layer. Ethanol exposure was administered to model prenatal alcohol exposure, and dopamine was applied to evaluate its protective effects.

Results: Ethanol exposure was found to disrupt the spatiotemporal properties of synchronized spontaneous neural network electrical activity and partially induce neuronal apoptosis. Conversely, dopamine treatment increased the frequency of neural network electrical activity and attenuated ethanol-induced apoptosis.

Conclusion: The findings suggest that ethanol disrupts neural network activity and induces apoptosis in the developing nervous system, while dopamine exerts a protective effect by modulating neural network activity and reducing apoptosis. These results contribute to understanding the mechanisms underlying FASD and offer potential therapeutic avenues for prevention and treatment.